Cryotherapy (freezing) or laser photocoagulation are occasionally used alone to wall off a small area of retinal detachment so that the detachment does not spread.

The treatment method used depends on the cause of the hemorrhage. In most cases, the patient is advised to rest with the head elevated 30–45°, and sometimes to put patches over the eyes to limit movement prior to treatment in order to allow the blood to settle. The patient is also advised to avoid taking medications that cause blood thinning (such as aspirin or similar medications).

The goal of the treatment is to fix the cause of the hemorrhage as quickly as possible. Retinal tears are closed by Laser treatment or cryotherapy, and detached retinas are reattached surgically.

Even after treatment, it can take months for the body to clear all of the blood from the vitreous. In cases of vitreous hemorrhage due to detached retina,long-standing vitreous hemorrhage with a duration of more than 2–3 months, or cases associated with rubeosis iridis or glaucoma, a vitrectomy may be necessary to remove the standing blood in the vitreous.

Scleral buckle surgery is an established treatment in which the eye surgeon sews one or more silicone bands (or tyres) to the sclera (the white outer coat of the eyeball). The bands push the wall of the eye inward against the retinal hole, closing the break or reducing fluid flow through it and reducing the effect of vitreous traction thereby allowing the retina to re-attach. Cryotherapy (freezing) is applied around retinal breaks prior to placing the buckle. Often subretinal fluid is drained as part of the buckling procedure. The buckle remains in situ. The most common side effect of a scleral operation is myopic shift. That is, the operated eye will be more short sighted after the operation. Radial scleral buckle is indicated for U-shaped tears or Fishmouth tears, and posterior breaks. Circumferential scleral buckle is indicated for multiple breaks, anterior breaks and wide breaks. Encircling buckles are indicated for breaks covering more than 2 quadrants of retinal area, lattice degeneration located on more than 2 quadrant of retinal area, undetectable breaks, and proliferative vitreous retinopathy.

Though no topical treatment has been proven to be effective in the treatment of Central Serous Retinopathy. Some doctors have attempted to use nonsteroidal topical medications to reduce the subretinal fluid associated with CSR. The nonsteroidal topical medications that are sometimes used to treat CSR are, Ketorolac, Diclofenac, or Bromfenac.

While surgeries do exist to correct for severe cases of floaters, there are currently no medications (including eye drops) that can correct for this vitreous deterioration. Floaters are often caused by the normal aging process and will usually disappear as the brain learns to ignore them. Looking up/down and left/right will cause the floaters to leave the direct field of vision as the vitreous humour swirls around due to the sudden movement. If floaters significantly increase in numbers and/or severely affect vision, then one of the below surgeries may be necessary.

Currently, insufficient evidence is available to compare the safety and efficacy of surgical vitrectomy with laser vitreolysis for the treatment of floaters. A 2017 Cochrane Review did not find any relevant studies that compared the two treatments.

Aggressive marketing campaigns are currently promoting the use of laser vitreolysis for the treatment of floaters. No strong evidence currently exists for the treatment of floaters with laser vitreolysis. Currently, the strongest available evidence comparing these two treatment modalities are retrospective case series.

People who have irregular sleep patterns, type A personalities, sleep apnea, or systemic hypertension are more susceptible Central Serous Retinopathy, as stated in Medscape “The pathogenesis here is thought to be elevated circulating cortisol and epinephrine, which affect the autoregulation of the choroidal circulation,” With management of these lifestyle patterns, it has been shown that the fluid associated with Central Serous Retinopathy can spontaneously resolve with the management of the cortisol and epinephrine levels. Melatonin has been shown to help regulate sleep in people who have irregular sleep patterns (such as 3rd shift workers, or overnight employees), in turn regulating cortisol and epinephrine levels to manage CSR.

Enzymatic vitreolysis has been trialled to treat vitreomacular traction (VMT) and anomalous posterior vitreous detachment. Whilst the mechanism of action may have an effect on clinically significant floaters, as of March 2015 there are no clinical trials being undertaken to determine whether this may be a therapeutic alternative to either i) conservative management, or ii) vitrectomy.

Optic pits themselves do not need to be treated. However, patients should follow up with their eye care professional annually or even sooner if the patient notices any visual loss whatsoever. Treatment of PVD or serous retinal detachment will be necessary if either develops in a patient with an optic pit.

Surgeons can remove or peel the membrane through the sclera and improve vision by 2 or more Snellen lines. Usually the vitreous is replaced at the same time with clear (BSS) fluid, in a vitrectomy. Surgery is not usually recommended unless the distortions are severe enough to interfere with daily living, since there are the usual hazards of surgery, infections, and a possibility of retinal detachment. More common complications are high intraocular pressure, bleeding in the eye, and cataracts, which are the most frequent complication of vitrectomy surgery. Many patients will develop a cataract within the first few years after surgery. In fact, the visual distortions and diplopia created by cataracts may sometimes be confused with epiretinal membrane.

Barrage laser is at times done prophylactically around a hole or tear associated with lattice degeneration in an eye at risk of developing a retinal detachment. It is not known if surgical interventions such as laser photocoagulation or cryotherapy is effective in preventing retinal detachment in patients with lattice degeneration or "asymptomatic" retinal detachment. Laser photocoagulation has been shown to reduce risks of retinal detachment in "symptomatic" lattice degeneration. There are documented cases wherein retina detached from areas which were otherwise healthy despite being treated previously with laser.

Retinal haemorrhages, especially mild ones not associated with chronic disease, will normally resorb without treatment. Laser surgery is a treatment option which uses a laser beam to seal off damaged blood vessels in the retina. Anti-vascular endothelial growth factor (VEGF) drugs like Avastin and Lucentis have also been shown to repair retinal haemorrhaging in diabetic patients and patients with haemorrhages associated with new vessel growth.

Risk factors such as UVB exposure and smoking can be addressed. Although no means of preventing cataracts has been scientifically proven, wearing sunglasses that counteract ultraviolet light may slow their development. While adequate intake of antioxidants (such as vitamins A, C, and E) has been thought to protect against the risk of cataracts, clinical trials have shown no benefit from supplements; though evidence is mixed, but weakly positive, for a potential protective effect of the nutrients lutein and zeaxanthin. Statin use is somewhat associated with a lower risk of nuclear sclerotic cataracts.

Therapy is not required or indicated in posterior vitreous detachment, unless there are associated retinal tears, which need to be repaired. In absence of retinal tears, the usual progress is that the vitreous humor will continue to age and liquefy and floaters will usually become less and less noticeable, and eventually most symptoms will completely disappear. Prompt examination of patients experiencing vitreous humor floaters combined with expeditious treatment of any retinal tears has been suggested as the most effective means of preventing certain types of retinal detachments.

The postoperative recovery period (after removing the cataract) is usually short. The patient is usually ambulatory on the day of surgery, but is advised to move cautiously and avoid straining or heavy lifting for about a month. The eye is usually patched on the day of surgery and use of an eye shield at night is often suggested for several days after surgery.

In all types of surgery, the cataractous lens is removed and replaced with an artificial lens, known as an intraocular lens, which stays in the eye permanently. Intraocular lenses are usually monofocal, correcting for either distance or near vision. Multifocal lenses may be implanted to improve near and distance vision simultaneously, but these lenses may increase the chance of unsatisfactory vision.

Careful eye examination by an ophthalmologist or optometrist is critical for diagnosing symptomatic VMA. Imaging technologies such as optical coherence tomography (OCT) have significantly improved the accuracy of diagnosing symptomatic VMA.

A new FDA approved drug was released on the market late 2013. Jetrea (Brand name) or Ocriplasmin (Generic name) is the first drug of its kind used to treat vitreomacular adhension.

Mechanism of Action: Ocriplasmin is a truncated human plasmin with proteolytic activity against protein components of the vitreous body and vitreretinal interface. It dissolves the protein matrix responsible for the vitreomacular adhesion.

Adverse drug reactions: Decreased vision, potential for lens sublaxation, dyschromatopsia (yellow vision), eye pain, floaters, blurred vision.

New Drug comparison Rating gave Jetea a 5 indicating an important advance.

Previously, no recommended treatment was available for the patient with mild symptomatic VMA. In symptomatic VMA patients with more significant vision loss, the standard of care is pars plana vitrectomy (PPV), which involves surgically removing the vitreous from the eye, thereby surgically releasing the symptomatic VMA. In other words, vitrectomy induces PVD to release the traction/adhesion on the retina. An estimated 850,000 vitrectomy procedures are performed globally on an annual basis with 250,000 in the United States alone.

A standard PPV procedure can lead to serious complications including small-gauge PPV. Complications can include retinal detachment, retinal tears, endophthalmitis, and postoperative cataract formation. Additionally, PPV may result in incomplete separation, and it may potentially leave a nidus for vasoactive and vasoproliferative substances, or it may induce development of fibrovascular membranes. As with any invasive surgical procedure, PPV introduces trauma to the vitreous and surrounding tissue.

There are data showing that nonsurgical induction of PVD using ocriplasmin (a recombinant protease with activity against fibronectin and laminin) can offer the benefits of successful PVD while eliminating the risks associated with a surgical procedure, i.e. vitrectomy. Pharmacologic vitreolysis is an improvement over invasive surgery as it induces complete separation, creates a more physiologic state of the vitreomacular interface, prevents the development of fibrovascular membranes, is less traumatic to the vitreous, and is potentially prophylactic. As of 2012, ThromboGenics is still developing the ocriplasmin biological agent. Ocriplasmin is approved recently under the name Jetrea for use in the United States by the FDA.view.

An experimental test of injections of perfluoropropane (CF) on 15 symptomatic eyes of 14 patients showed that vitreomacular traction resolved in 6 eyes within 1 month and resolved in 3 more eyes within 6 months.

In the early stages, there are a few treatment options. Laser surgery or cryotherapy (freezing) can be used to destroy the abnormal blood vessels, thus halting progression of the disease. However, if the leaking blood vessels are clustered around the optic nerve, this treatment is not recommended as accidental damage to the nerve itself can result in permanent blindness. Although Coats' disease tends to progress to visual loss, it may stop progressing on its own, either temporarily or permanently. Cases have been documented in which the condition even reverses itself. However, once total retinal detachment occurs, sight loss is permanent in most cases. Removal of the eye (enucleation) is an option if pain or further complications arise.

There is no good evidence for any preventive actions, since it appears this is a natural response to aging changes in the vitreous. Posterior vitreous detachment (PVD) has been estimated to occur in over 75 per cent of the population over age 65, that PVD is essentially a harmless condition (although with some disturbing symptoms), and that it does not normally threaten sight. However, since epiretinal membrane appears to be a protective response to PVD, where inflammation, exudative fluid, and scar tissue is formed, it is possible that NSAIDs may reduce the inflammation response. Usually there are flashing light experiences and the emergence of floaters in the eye that herald changes in the vitreous before the epiretinal membrane forms g

Anti-muscarinic topical medications in children under 18 years of age may slow the worsening of myopia. These treatments include pirenzepine gel, cyclopentolate eye drops, and atropine eye drops. While these treatments were shown to be effective in slowing the progression of myopia, side effects included light sensitivity and near blur.

If caught early, the neovascularization can be reversed with prompt pan retinal photocoagulation (PRP), or injection of anti-VEGF medications with subsequent PRP. The injection blocks the direct effect of VEGF and acts more quickly but will wear off in about 6 weeks. PRP has a slower onset of action but can last permanently. Once the neovascularization has been longstanding, the new vessels recruit fibrous tissue, and as this forms and contracts, the angle can be permanently damaged, and will not respond to treatment. If this occurs, then surgical intervention is required to reduce the pressure (such as a glaucoma drainage implant)

Scleral reinforcement surgery is aimed to cover the thinning posterior pole with a supportive material to withstand intraocular pressure and prevent further progression of the posterior staphyloma. The strain is reduced, although damage from the pathological process cannot be reversed. By stopping the progression of the disease, vision may be maintained or improved.

Several options exist for the treatment of BRVO. These treatments aim for the two of the most significant complications of BRVO, namely macular edema and neovascularization.

- Systemic treatment with oral Aspirin, subcutaneous Heparin, or intravenous thrombolysis have not been shown to be effective treatments for CRVO and for BRVO no reliable clinical trial has been published.

- Laser treatment of the macular area to reduce macular edema is indicated in patients who have 20/40 or worse vision and did not spontaneously improve for at least 3 months (to permit the maximum spontaneous resolution) after the development of the vein occlusion. It is typically administered with the argon laser and is focused on edematous retina within the arcades drained by the obstructed vein and avoiding the foveal avascular zone. Leaking microvascular abnormalities may be treated directly, but prominent collateral vessels should be avoided.

- The second indication of laser treatment is in case of neovascularization. Retinal photocoagulation is applied to the involved retina to cover the entire involved segment, extending from the arcade out to the periphery. Ischemia alone is not an indication for treatment provided that follow-up could be maintained.

- Preservative-free, nondispersive Triamcinolone acetonide in 1 or 4 mg dosage may be injected into the vitreous to treat macular edema but has complications including elevated intraocular pressure and development of cataract. Triamcinolone injection is shown to have similar effect on visual acuity when compared with standard care (Laser therapy), However, the rates of elevated intraocular pressure and cataract formation is much higher with the triamcinolone injection, especially the higher dosage. Intravitreal injection of Dexamethasone implant (Ozurdex; 700,350 μg) is being studied, its effect may last for 180 days. The injection may be repeated however with less pronounced effect. Although the implant was designed to cause less complications, pressure rise and cataract formation is noted with this treatment too.

- Anti-VEGF drugs such as Bevacizumab (Avastin; 1.25 -2.5 mg in 0.05ml) and Ranibizumab (lucentis) injections are being used and investigated. Intravitreal anti-VEGFs have a low incidence of adverse side effects compared with intravitreal corticosteroids, but are currently short acting requiring frequent injections. Anti-VEGF injection may be used for macular edema or neovascularization. The mechanism of action and duration of anti-VEGF effect on macular edema is currently unknown. The intraocular levels of VEGF are increased in eyes with macular edema secondary to BRVO and the elevated VEGF levels are correlated to the degree and severity of the areas of capillary nonperfusion and macular edema.

- Surgery is employed occasionally for longstanding vitreous hemorrhage and other serious complications such as epiretinal membrane and retinal detachment.

- Arteriovenous sheathotomy has been reported in small, uncontrolled series of patients with BRVO. BRVO typically occurs at arteriovenous crossings, where the artery and vein share a common adventitial sheath. In arteriovenous sheathotomy an incision is made in the adventitial sheath adjacent to the arteriovenous crossing and is extended along the membrane that holds the blood vessels in position to the point where they cross, the overlying artery is then separated from the vein.

In terms of the treatment of cytomegalovirus retinitis, oral valganciclovir, intravenous ganciclovir, IV foscarnet, and IV cidofovir are all efficient in the treatment of this condition. Also intravitreal injections, an injection of medicine into the vitreous near the retina, of foscarnet in concomitance with oral valganciclovir can be used for treatment as well.

Often individuals with CMV retinitis will need surgery for either retinal detachment or intravitreal instillation of ganciclovir. Retinal detachment occurs in up to 29% of affected eyes, repair being most effective with endolaser and silicone oil endotamponade.Intravitreal ganciclovir implant has the benefit of less systemic toxicity. An adverse effect of this is retinal detachment (and vitreous hemorrhage), also there is no systemic beneficial effect for cytomegalovirus organ disease.

There are good results from multiple doses of intravitreal injections of anti-VEGF drugs such as bevacizumab. A 2017 systematic review update found moderate evidence that aflibercept may have advantages in improving visual outcomes over bevacizumab and ranibizumab, after one year. Present recommended treatment for diabetic macular edema is Modified Grid laser photocoagulation combined with multiple injections of anti-VEGF drugs.

Peri-ocular injection of corticosteroids (injection of corticosteroids very close but not into the eye). In resistant cases oral administration of corticosteroids, immunosuppressive drugs, and laser or cryotherapy of the involved area may be indicated.

Steroid implants have been explored as a treatment option for individuals with non-infectious uveitis. Research comparing fluocinolone acetonide intravitreal implants to standard-of-care treatments (prednisolone with immunosuppressive agents) found that while the steroid implant treatment possibly prevents the recurrence of uveitis, there may be adverse safety outcomes, such as the increased risk for needing cataract surgery and surgery to lower intraocular pressure.

To date, there is no known effective treatment for the non-proliferative form of macular telangiectasia type 2.

Treatment options are limited. No treatment has to date been shown to prevent progression. The variable course of progression of the disease makes it difficult to assess the efficacy of treatments. Retinal laser photocoagulation is not helpful. In fact, laser therapy may actually enhance vessel ectasia and promote intraretinal fibrosis in these individuals. It is hoped that a better understanding of the pathogenesis of the disease may lead to better treatments.

The use of vascular endothelial growth factor (VEGF) inhibitors, which have proven so successful in treating age-related macular degeneration, have not proven to be effective in non-proliferative MacTel type 2. Ranibizumab reduces the vascular leak seen on angiography, although microperimetry suggests that neural atrophy may still proceed in treated eyes.In proliferative stages (neovascularisation), treatment with Anti-VEGF can be helpful.

CNTF is believed to have neuroprotective properties and could thus be able to slow down the progression of MacTel type 2. It has been shown to be safe to use in MacTel patients in a phase 1 safety trial.